Metastasis is the major cause of treatment failure in various type of cancer and particularly in breast cancer patients. The extracellular matrix glycophosphoprotein osteopontin (OPN) is normally secreted by osteoblasts and is utilised as an extracellular adhesion molecule. Osteopontin has also been associated with certain aspects of malignant transformation (1) by enhancing malignant cell attachment and migration and contributing to anchorage-independent growth of tumour cells (2, 3). Transfection of benign, non-metastatic rat mammary cells with cDNA for OPN has been determined to endow the transfectants with the ability to overproduce OPN in vitro and to metastatsize in vivo (4). OPN overexpression has been associated with poor prognosis in human primary breast cancer (5, 6) and OPN has been shown to be the single most powerful prognostic factor in a multivariate analysis against outcome, in a large prospective study of breast cancer patients (7). Although it is known that circulating plasma levels of OPN are higher in metastatic breast cancer patients (8), the precise molecular mechanisms of OPN regulated metastasis remains unclear.